Science

Pipeline

Upstream innovation

COMBINING EARLY IMMUNE INTERVENTION WITH ANTIFIBROTIC THERAPY

Traditional therapies for interstitial lung diseases focus on treating the fibrotic end stage, once irreversible lung damage has already occurred.  At A.D.A., we take a different approach by intervening early — at the origin of the disease. It is increasingly recognized that many ILDs have an autoimmune component driving their pathogenesis. Although the exact cause of idiopathic pulmonary fibrosis (IPF) remains unknown, there is an increasing amount of evidence showing that early immune-mediated inflammation triggers fibrosis. Our strategy targets these early inflammatory signals to prevent fibrosis progression. By modulating immune responses prior to the cascade leading to fibrosis, we aim to reduce fibrotic changes, preserving lung function and improving patient outcomes, offering a promising alternative to conventional therapies for complex pulmonary conditions.

Our innovative “Drug AND Delivery” platform not only modulates the underlying immune response, but uniquely offers the capability to incorporate an antifibrotic molecule within the same delivery system. This dual-action approach allows us to address simultaneously the autoimmune trigger and its fibrotic manifestations, ultimately preserving lung function and improving patients’ lives.

Myofibroblasts deposit excess ECM, which increases tissue stiffness and impairs gas exchange. This, in turn, results in further lung injury and fibroblast activation, perpetuating a self-sustaining activation loop that ultimately drives PPF and remodeling of the lung structure

Fibroblasts proliferate and migrate to the site of injury, where they are activated

White blood cells infiltrate the site of injury and release pro-inflammatory cytokines to support tissue repair, as well as profibrotic mediators that promote the activation of fibroblasts

The profibrotic microenvironment promotes the differentiation of fibroblasts to myofibroblasts, which play a major role in excess fibrosis

Myofibroblasts deposit excess ECM, which increases tissue stiffness and impairs gas exchange. This, in turn, results in further lung injury and fibroblast activation, perpetuating a self-sustaining activation loop that ultimately drives PPF and remodeling of the lung structure

Fibroblasts proliferate and migrate to the site of injury, where they are activated

White blood cells infiltrate the site of injury and release pro-inflammatory cytokines to support tissue repair, as well as profibrotic mediators that promote the activation of fibroblasts

The profibrotic microenvironment promotes the differentiation of fibroblasts to myofibroblasts, which play a major role in excess fibrosis

Product

Pre-clinical

Ph. I

Ph. II - III

ADA001

IPF

Mono-therapy
ADA002

(CTD-ILD*)

Mono-therapy
ADA003

(CTD-ILD* & IPF)

Combination therapy

* currently focus on SSc-ILD model

Product

Pre-clinical

Ph. I

Ph. II - III

ADA001
IPF
Mono-therapy
ADA002
(CTD-ILD*)
Mono-therapy
ADA003
(CTD-ILD* & IPF)
Combination therapy

* currently focus on SSc-ILD model

ADA001

Integrated therapeutic strategy: empowering TGF-Beta inhibition by antifibrotic carrier

ADA001 is an inhaled formulation that incorporates a potent TGF-β inhibitor within an amphiphilic carrier. This efficiently transports the active agent and exerts its own intrinsic antifibrotic effects. 

The dual-action mechanism enhances the modulation of TGF-β signalling while mitigating fibrotic processes.

ADA002

Mycophenolic acid nanoparticles: a breakthrough in immunomodulatory delivery

We have developed a groundbreaking drug candidate based on a self-assembling nanoparticle system composed entirely of mycophenolic acid (MPA). MPA effectively modulates immune responses by selectively inhibiting lymphocyte proliferation; it is a critical component of therapies aimed at controlling overactive immune activity. MPA is a potent immunosuppressant functioning…

as noncompetitive, selective and reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH). Transforming MPA into a self-assembling nanoparticle offers substantial advantages over traditional formulations: it ensures improved delivery to target tissues by significantly enhancing mucus penetration—a fundamental requirement in developing inhaled therapies for ILDs. Additionally, it provides enhanced MPA bioavailability, increasing its aqueous solubility by over 70 times.

ADA003

Dual-Target nanoparticle therapy: targeting fibrotic pathways and immune hyperactivation

We developed a combination therapy by encapsulating an antifibrotic agent into our self-assembling nanoparticles (ADA002). This unified approach targets simultaneously two key therapeutic areas: the fibrotic manifestations and the…

underlying hyperactivation of the immune system, addressing both the structural and immunological aspects of the disease.

Patent

Lead candidate ADA002

Patent number n° 102023000006933 (patent pending) – Nanoparticles of Mycophenolic acid prodrug molecules and therapeutic use thereof

Lead candidate ADA001

Lead candidate ADA001: Patent number n° 102024000025392 (patent pending) – TGF-beta receptor inhibitors for use in the therapeutic treatment of fibrotic lung disease